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CONGESTIVEHEART FAILURE


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INTRODUCTION

Heart (or cardiac) failure:pathophysiological state in

which the heart is unable to pump blood at a rate

commensurate with the requirements of the metabolizing

tissues or can do so only from an elevated filling pressure

Congestive heart failure (CHF): complex clinical

syndrome characterized by abnormalities of left

ventricular function and neurohormonal regulation, which

are accompanied by effort intolerance, fluid retention, and

reduced longevity


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Etiology It is a common end point for many diseases ofcardiovascular system

It can be caused by :-Inappropriate work load (volume or pressure

overload)

-Restricted filling

-Myocyte loss


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Causes of left ventricular failure

Volume over load: Regurgitate valve

High output status

Pressure overload: Systemic hypertension

Outflow obstruction

Loss of muscles: Post MI, Chronic ischemia

Connective tissue diseases

Infection, Poisons (alcohol, cobalt)

Restricted Filling: Pericardial diseases, Restrictive

cardiomyopathy, tachyarrhythmia


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According to AHA,

CHF is a clinical syndrome that can result from any

structural or functional cardiac disorder that impairsthe ability of the ventricle to fill with or eject blood

Heart failure (HF) may be acute or chronic

i) acute HF

ii) chronic HF (CHF)


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CHRONIC HEART FAILURE

CHF develops in following states:

i) myocardial ischaemia from atherosclerotic coronary arterydisease

ii) multivalvular heart disease

iii) systemic arterial hypertension

iv) chronic lung disease resulting in hypoxia, pulmonary arterialhypertension

v) progression of acute into chronic failure


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In chronic heart failure, compensatory mechanisms

like tachycardia, cardiac dilatation and cardiachypertrophy try to make adjustments so as to

maintain adequate cardiac output

Clinical manifestations of heart failure result from

the accumulation of excess fluid to the left or right

cardiac chamber, whichever is initially affected


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Heart disease(any)

HypertensionDiabetes,

Hypercholesterolemia

AsymptomaticLV dysfunction

Systolic / Diastolic

Marked symptoms

at rest despite

max. therapy

Dyspnea, Fatigue

Reduced exercisetolerance

Stages in the Evolution of Heart Failure

A

B

C

D

AHA guidelines 2001


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Left-sided Heart Failure

Initiated by stress to the left heart

The major causes are:

i) systemic hypertension

ii) mitral or aortic valve disease (stenosis)

iii) Ischaemic heart disease

iv) Myocardial diseases e.g. cardiomyopathies, myocarditis

v) Restrictive pericarditis


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Result from accumulation of fluid in the lungs and

from decreased left ventricular output

Major pathological changes are:

i) pulmonary congestion and oedema, causing dyspnoea andorthopenia

ii) decreased left ventricular output causing hypoperfusion and

diminished oxygenation of tissues


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Right-sided Heart Failure

consequence of left side heart failure

The major causes are:

i) as a consequence of left ventricular failure

ii) intrinsic lung diseases

iii) pulmonary or tricuspid valvular disease

iv) pulmonary hypertensionv) myocardial diseases affecting right side of heart


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Left heart failure

IHD, Myocarditis,

Valvular heart diseases

Forward failureBackward failure

cardiac output

Tissue anoxia

renal perfusion

Activation of RAAS

PULMONARY

CONGESTION and

OEDEMA

Na+, H2O retention

Residual blood in left ventricle

Left atrial pressure and volume

Pressure in pulmonary venous circulation

Pulmonary arterial hypertension

Right ventricular pressure

SYSTEMIC VENOUS

CONGESTION and

PERIPHERAL OEDEMA

Right heart failure

Right side valvular disease

Rt side myocardial disease

Pulmonary hypertension


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Activation of NA, ANP

Tachycardia

CONGESTIVE

HEART FAILURE

Further stress on myocardium

Myocardial contractility

cardiac workload

Cell stretching

COMPENSATORY

HYPERTROPHY and

DILATATION

COMPENSATORY MECHANISMS

Lt. VENTRICULAR FAILURE

IHD, Myocardits,Valvular heartdisease

Rt. VENTRICULAR FAILURE

Pulmonary HT, Valvular heartdisease

Activation of RAAS

mechanism

Na+ and water

retention


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Pathophysiology

Hemodynamic changes

Neurohormonal changes

Cellular changes


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Hemodynamic changes

HF can be secondary to systolic dysfunction ordiastolic dysfunction


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Neurohormonal changes

N/H changes Favorable effect Unfavorable effect

Sympathetic activity HR , contractility,vasoconst. V return,

filling

Arteriolar constriction

After load workload

O2 consumption

Renin-AngiotensinAldosterone

Salt & water retention

VR

Vasoconstriction

after load

Vasopressin Same effect Same effect

interleukins &TNF- May have roles in myocytehypertrophy

Apoptosis

Endothelin VasoconstrictionVR After load


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Cellular changes

Changes in Ca+2handling

Changes in adrenergic receptors:

Slight in 1 receptors

1 receptors desensitization

followed by downregulation

Changes in contr acti le proteins

Program cell death (Apoptosis)

I ncrease amount of f ibrous tissue


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Symptoms

Orthopnea, paroxysmal nocturnal dyspnea

Low cardiac output symptoms

Abdominal symptoms: Anorexia,nausea,

Abdominal fullness,

Rt hypochondrial pain

Pale cold sweaty skin


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Swelling of the ankles, legs, and hands

Orthopnea, or the shortness of breath

when lying flat

Shortness of breath during exertion


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Symptoms

(involving circulation)

Cyanosis, or a bluish color that is seen in the lips and

fingernails from a lack of oxygen

Fatigue or weakness

Rapid or irregular heart beat

Changes of behavior such as restlessness, confusion,

and decreased attention span


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Symptoms

(involving congestion)

Unexplained or unintentional weight gain

Chronic cough

Increased urination

Loss of appetite or indigestion


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Congestive heart failure is a syndrome that can be

caused by multiple underlying diseases such as:

Congenital heart disease Atherosclerosis

Rheumatic fever

Cardiomyopathy

Valve disorders

Ventricular failure

Left or right-sided failure

Hypertension Prolonged alcohol or drug addiction

Previous heart attack

Diabetes

Chronic rapid heartbeats

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